Association between glucose variability and postoperative delirium in acute aortic dissection patients: an observational study.

BACKGROUND: Blood glucose variability is associated with poor prognosis after cardiac surgery, but the relationship between glucose variability and postoperative delirium in patients with acute aortic dissection is unclear. The study aims to investigate the association of blood glucose variability with postoperative delirium in acute aortic dissection patients. METHODS: We prospectively analyzed 257 patients including 103 patients with delirium. The patients were divided into two groups according to whether delirium was present. The outcome measures were postoperative delirium, the length of the Intensive Care Unit stay, and the duration of hospital stay. Multivariable Cox competing risk survival models was used to assess. RESULTS: A total of 257 subjects were enrolled, including 103 patients with delirium. There were statistically significant differences between the two groups in body mass index, history of cardiac surgery, first admission blood glucose, white blood cell counts, Acute Physiology and Chronic Health Evaluation II score, hypoxemia, mechanical ventilation duration, and the length of Intensive Care Unit stay(P < 0.05). The delirium group exhibited significantly higher values of the mean of blood glucose (MBG) and the standard deviation of blood glucose (SDBG) than in the non-delirium group(P < 0.05). In model 1, the adjusted hazard ratio (AHR) of the standard deviation of blood glucose was 1.436(P < 0.05). In Model 2, the standard deviation of blood glucose (AHR = 1.418, 95%CI = 1.195-1.681, P < 0.05) remained significant after adjusting for confounders. The area under the curve of the SDBG was 0.763(95%CI = 0.704-0.821, P < 0.01). The sensitivity was 81.6%, and the specificity was 57.8%. CONCLUSIONS: Glucose variability is associated with the risk of delirium in patients after aortic dissection surgery, and high glycemic variability increases the risk of postoperative delirium.

[Roles of hypertension and serum leptin in obstructive sleep apnea hypopnea syndrome].

OBJECTIVE: To explore the roles of hypertension and serum leptin in obstructive sleep apnea hypopnea syndrome (OSAHS). METHODS: Totally 60 patients with OSAHS (OSAHS group) and 40 age- and body mass index (BMI)-matched non-OSAHS individuals (non-OSAHS group) were enrolled in this study. The neck circumference (NC), waist/hip rate (WHR), systolic blood pressure (SBP), diastolic blood pressure (DBP), leptin, fasting blood glucose (FBG), triglyceral (TG), cholesterol (Chol), and true insulin (TI) were measured before and after sleep . The correlations between hypertension/serum leptin level and OSAHS were analyzed. RESULTS: The blood pressure(in the morning), especially DBP was significantly higher in OSAHS group than in non-OSAHS control group (89.75+/-2.04) mmHg vs. (81.63+/-1.91) mmHg, P<0.01. DBP in OSAHS group was positively correlated with serum leptin and apnea hypopnea index (AHI) (r=0.282, P<0.05; r=0.318, P<0.01). Logistic regression analysis showed that BMI (P=0.029), heart rate in the morning (P =0.030), and leptin (P=0.049) were independently correlated with the development of hypertension. CONCLUSIONS: OSAHS may independently affect blood pressure, especially DBP, after waking up. BMIHR in the morning and serum leptin may be the independent correlates of hypertension.

[The effects of overnight sleep deprivation on cardiovascular autonomic modulation].

OBJECTIVE: This study aimed to delineate cardiovascular autonomic modulation associated with overnight total sleep deprivation (TSD) in humans. METHODS: Cardiovascular autonomic modulation during overnight total sleep deprivation was assessed in 18 normal male subjects [age: (26.2 +/- 4.2) years, BMI (23.9 +/- 1.7) kg/m(2)]. ECG and continuous blood pressure from radial artery tonometry were obtained in seated position before TSD (baseline) and after overnight TSD. Spectral analysis of heart rate variability (HRV) and BP variability (BPV) were computed for cardiac parasympathetic modulation (high frequency power, HF); sympathetic modulation (low frequency power, LF), sympatho-vagal balance (LF/HF power of R-R variability, LF/HF) and BPV sympathetic modulation (low frequency power, BPV LF) in normalized (N) units [(total power of the components)/(total power-very low frequency power) x 100]. RESULTS: No significant changes were found in BP and heart rate. HRV LF was increased significantly from baseline (59.4 +/- 15.7)% to overnight SD (67.0 +/- 13.9)%. HRV LF/HF was increased significantly from baseline (2.7 +/- 1.7) to overnight SD (3.8 +/- 2.3), HRV HFN was decreased from baseline (29.0 +/- 11.6)% to overnight SD (22.8 +/- 10.4)%, BPV LF was significantly increased from baseline (63.2 +/- 16.5)% to overnight SD (72.4 +/- 13.2)%. CONCLUSION: Acute SD was associated with increased sympathetic and decreased parasympathetic cardiovascular modulation.

Gastro-oesophageal reflux disease and respiratory disease.

An epidemiological survey showed that respiratory symptoms with gastro-oesophageal reflux (GER) were twice as high as those without GER symptoms. In 46 cases of unknown chronic cough or asthma, 67% had positive oesophageal pH monitoring. Of 34 patients with snoring and reflux symptoms, 16 (47.1%) were confirmed as positive for obstructive sleep apnoea (OSA) and GER. Anti-reflux therapy significantly improved both GER and OSA.

Cognitive and emotional impairment in obstructive sleep apnea syndrome.

OBJECTIVE: To evaluate the emotional and cognitive status in patients with obstructive sleep apnea syndrome (OSAS), using neuropsychological tests and evoked-related potential (P3). METHODS: Sixteen patients diagnosed of OSAS were tested by Hamilton rating scale for anxiety (HRSA) and Hamilton rating scale for depression (HRSD). Other three groups, OSAS patient group (n = 21), snoring group (n = 21), and control group (n = 21), were administered polysomnography (PSG), auditory evoked event-related potential (P3), and clinic memory test. The results were analyzed using general linear model (GLM) analysis and Post Hoc test. RESULTS: Twelve OSAS patients' scores of HRSA and HRSD were beyond the normal range, 26.42 +/- 4.48 and 22.08 +/- 3.97 respectively. The auditory P3 latency in OSAS group was 363.1 +/- 22.9 ms (Fz), 368.57 +/- 28.03 ms (Cz), in snoring group 336.57 +/- 31.08 ms (Fz), 339.81 +/- 31.76 ms (Cz), in control group 340.8 +/- 28.7 ms (Fz), 338.29 +/- 29.21 ms (Cz). There were significant differences between OSAS group and snoring group, as well as control group (P < 0.05). No significant difference was seen between snoring group and control group. No significant difference was noted in P3 amplitude among three groups. Memory quotient (MQ) reduced in snoring group compared with control group. CONCLUSIONS: Emotional disturbances are common clinical features in OSAS patients. Abnormal auditory P3 latency indicates the cognitive dysfunction in OSAS patients. Nocturnal hypoxaemia may play an important role on it. Snorers should be monitored because of the tendency to develop cognitive impairment.

[Relationship of changes in sleep architecture and cognitive function in patients with obstructive sleep apnea syndrome].

OBJECTIVES: To explore the relationship between sleep architecture changes and cognitive impairment in patients with obstructive sleep apnea syndrome (OSAS). METHODS: Thirty-six patients with OSAS and 18 controls were administered polysomnography and neuropsychological tests of visual regeneration, digital symbol, comprehensive memory and digital span. RESULTS: Performances on the visual regeneration test and digital symbol test in patients with OSAS were impaired significantly compared with the control group (P < 0.01). Patients' performance on the visual regeneration test was significantly associated with slow wave sleep duration (r = 0.423, P < 0.05) and that on the digital symbol test was significantly associated with REM sleep duration (r = 0.378, P < 0.05). CONCLUSIONS: Slow wave sleep and REM sleep derivation may play a role in the cognitive impairment in patients with OSAS.

[Effects of nasal continuous positive airway pressure on serum leptin concentration and the metabolic parameters in obstructive sleep apnea hypopnea syndrome].

OBJECTIVE: To evaluate the effects of nasal continuous positive airway pressure (nCPAP) on serum leptin concentration and the metabolic parameters in patients with obstructive sleep apnea/hypopnea syndrome (OSAHS). METHODS: Serum leptin levels and true insulin (TI) levels were measured before and after one night nCPAP therapy in 18 patients. Eight patients received regular nCPAP treatment and had no change of body weight (BMI change < or = 1.5 kg/m2 from baseline) were recruited to the reassessment study 7.5 months after therapy. RESULTS: After one night use of nCPAP, there was a significant decrease in serum leptin [(8.47 +/- 0.62) microg/L vs (7.32 +/- 0.64) microg/L, P = 0.022] without change in other parameters. After 7.5 months of nCPAP treatment, serum leptin levels continued to decrease significantly without changes in BMI [(8.35 +/- 0.83) microg/L vs (6.05 +/- 0.78) microg/L; P = 0.036), and fast blood glucose (FBG) and true insulin (TI) also decreased significantly (P = 0.036) in OSAHS patients. However, triglyceral (TG) and cholesterol (Chol) maintained the pretreatment level (P > 0.05). CONCLUSIONS: OSAHS may have significant effects on the serum leptin levels and the correction of sleep disordered breathing by nCPAP can reduce the serum leptin levels. Decrease of leptin was independent of BMI change. The glucose metabolic disturbance and insulin resistance in OSAHS were improved after 7.5 months of nCPAP treatment.

[An investigation of the relationship between Lepr gene Gln223Arg polymorphism and obstructive sleep apnea hypopnea syndrome].

OBJECTIVE: To investigate the relationship between leptin receptor (Lepr) gene Gln223Arg polymorphism and obstructive sleep apnea hypopnea syndrome (OSAHS). METHODS: The genotypes of Gln223Arg polymorphism in Lepr gene were determined by polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLP) assay in 181 unrelated subjects of North region "Han" population (including 78 non-OSAHS subjects and 103 OSAHS subjects). RESULTS: The OSAHS patients with GG genotype had significantly larger neck circumference (NC) than did OSAHS patients with (GA + AA) genotype (P = 0.031); The study revealed no difference in genotype of Gln223Arg polymorphism between OSAHS group and non-OSAHS group (P = 0.676); There was also no significant difference in body mass index (BMI), waist hip rate (WHR), blood pressure (Bp), leptin (Lep), true insulin (TI), fast blood glucose (FBG), triglyceral (TG), cholesterol (Chol) and polysomnography (PSG) between GG and (GA + AA) genotype of OSAHS patients (P > 0.05). CONCLUSIONS: Lepr gene Gln223Arg polymorphism may be involved in the regulation of the neck regional fat distribution in OSAHS patients. It is unlikely that Lepr gene Gln223Arg polymorphism may contribute to the pathogenesis of OSAHS.

[The relationship between the changes of upper airway and genioglossus muscle activity after the treatment with Snoreguard].

OBJECTIVE: To investigate the relationship between the changes of upper airway and genioglossus muscle activity after the treatment with Snoreguard. METHODS: 31 patients with OSAS or snoring were treated with Snoreguard Cephalometric analysis was carried out to compare the changes of the upper airway before and after the treatment. The relationship between the change in morphology and that of genioglossus muscle activity among 22 patients was investigated. RESULTS: (1) The size of upper airway decreased significantly with Snoreguard. SPP-SPPW increased from (9.14 +/- 3.79) mm to (12.36 +/- 3.74) mm and TB-TPPW increased from (10.63 +/- 3.71) mm to (11.90 +/- 4.33) mm. UC-LC decreased from (21.96 +/- 11.06) mm to (10.48 +/- 8.55) mm and H-MP decreased from (20.60 +/- 6.65) mm to (11.01 +/- 6.84) mm. (2) The size of upper airway in part of the patients decreased with Snoreguard, but good treatment efficiency remained. CONCLUSION: The mechanism of Snoreguard is caused by the mechanical enlargement of upper airway.